Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
???displayArticle.abstract???
The periodic albino of Xenopus laevis displays a transitory presence of black melanin pigment in the embryo but looses this during tadpole development. This mutation, involving a recessive allele, affects melanogenesis in dermal melanophore pigment cells. It has been suggested that the mutation is intrinsic to the melanophore cell itself or, alternatively, reflects malfunction in the neuroendocrine system that regulates melanophore cell function. This latter system, involving pituitarymelanotrope cells which produces alpha-melanophore stimulating hormone (alpha-MSH), is responsible for stimulating the production and dispersion of melanin pigment in dermal melanophores. The purpose of the present study was to determine to which degree the albinism is intrinsic to the melanophore or involves neuroendocrine malfunction. Experiments involved transplantation of presumptive melanophores from wild-type to albino embryos, and vice versa, immunocytochemical analysis of the albino neuroendocrine system and the creation of wild-type/albino parabiotic animals to determine if the neuroendocrine system of the albino can support melanotrope cell function. We show that the albino has a functional neuroendocrine system and conclude that the defect in the albino primarily affects the melanophore cell, possibly rendering it incapable of responding to alpha-MSH. It is also apparent from our results that in later stages of development the cellular environment of the melanotrope cell does become important to its development, but the nature of the critical cellular factors involved remains to be determined.
Fig. 1. Melanophores in stage 35/36 periodic albino Xenopus following neural crest
transfer of prospective melanophores from a wild-type animal at stage 19/20.
Melanophores are in an expanded state of pigment dispersion in the stage 35/36
periodic albino host (arrow). Insert: Diagram of a stage 19/20 embryo indicating the
site of the donor–host tissue exchange (box). Scale Bars = 0.5 mm.
Fig. 2. Stage 42 tadpoles after stage 19/20 neural crest exchange and subsequent growth on a black background with constant overhead illumination. (A, B) Periodic albino
host that received wild-type neural crest tissue. All melanophores are in the punctuated form despite maintenance of the animals on a black background under continued
illumination. (C, D) Wild-type host with periodic albino neural crest tissue. Most melanophores exhibit dispersed melanin, but a few melanophores (arrow tips in D) remain
punctuate and are assumed to be of periodic donor origin. Scale Bars = 0.5 mm.
Fig. 3. Parasagittal immunocytochemical localization of a-MSH in the stage 42 periodic albino pituitary. (A) and (B) Hematoxylin–eosin stained parasagittal section of a stage
42 periodic albino brain. This orientation allows one to distinguish the anteriorpituitary from the pars intermedia (p.i). (C) Adjacent parasagittal brain section stained for a-
MSH. Note that only the pars intermedia exhibits a-MSH immunoreactivity. N, notochord; OC, optic chiasma. Scale Bar = 100 lm.
Fig. 4. Parabiosis of wild-type and periodic albino Xenopus. (A) Parabiosis between a periodic albino and a hypophysectomized wild-type embryo. Note the punctuate
melanophores in the head region of the wild-type partner, indicating removal of the pituitary. (B) The tail region of the parabiotic animals near the site of fusion. Note the
expanded melanophores within the tail region of the wild-type animal. (C) Parabiosis between a wild-type and periodic albino embryo with both partners having a pituitary.
Note expanded melanophores in head region of the normal partner. (D) The tail region of the parabiotic animals near the site of fusion. Note the expanded melanophores
within the tail region of the wild-type animal. Scale Bars = 0.5 mm.
